Functional medial thickening and folding of the internal elastic lamina in coronary spasm

Abstract

Although there are a number of studies on vasospastic angina, the structural changes at the cellular level that occur in the coronary arterial wall during spasm are not well known. Coronary spasm was induced by brushing the coronary adventitia in nine anesthetized beagles, and structural changes in the spastic coronary segments were examined by light and electron microscopy, making comparisons with the adjacent nonspastic segments. The % diameter stenosis of the spastic segments as measured angiographically was 79.4 Ϯ 12% (mean Ϯ SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 m (P Ͻ 0.0001) and % diameter and % area stenoses of spastic segment 81.0% and 96.5%, respectively, indicating that spasm was induced by medial thickening. Circular smooth muscle cells (SMCs) in the media were arranged in parallel with the internal (IEL) and external (EEL) elastic lamina in nonspastic segments but radially rearranged in spastic segments. SMCs were classified by their patterns of connection to IEL into six types by electron microscopy. Of these, three contracted and pulled the IEL toward the EEL, causing folding of the IEL and waving of EEL resulting in thickening of the media and narrowing of the lumen. We conclude that coronary spasm was elicited by radial rearrangement of the medial SMCs due to their own contraction and resultant medial thickening and folding of IEL, creating a piston effect to narrow the lumen, i.e., spasm. smooth muscle cell rearrangement CORONARY SPASM IS THE CAUSE of vasospastic angina. Coronary spasm is thought to be provoked by excessive contraction of circular smooth muscle cells (SMCs) present in the media of the coronary artery.Since medial SMCs can shorten their length by contraction by 30% at most, to attain a luminal narrowing of Ն75% is theoretically difficult without the existence of a thickened intima if their circular arrangement is not altered during contraction. Two concepts have been proposed as to the structural (morphological) mechanisms underlying coronary spasm: concentric narrowing of the coronary lumen in the presence of diffuse intimal thickening (6, 9, 12) and eccentric narrowing of the lumen in the presence of eccentric intimal thickening (2). However, no definitive evidence has emerged to support whether either of these mechanisms actually occurs clinically.There are a number of studies on humoral factors that participate in coronary spasm (7,15). Structural changes at the cellular level that occur in the coronary media during spasm, however, have not been clarified, probably because of the difficulty in analyzing coronary arterial architecture during spasm in patients and the lack of appropriate animal models of coronary spasm.Coronary spasm occurs not only in the large epicardial coronary arteries, often the site of atherosclerotic intimal thickening, but also in arterioles in which intimal thickening infrequently occurs (13). It is therefore necessary to elucidate the mechanisms of coronary spasm that oc...

Specific Shrinkage of Carotid Forks in Moyamoya Disease: A Novel Key Finding for Diagnosis

“…Very interestingly, Uchida et al (2011) produced a model of coronary artery spasm in the beagles and found that the internal elastic lamina are markedly folded like the “bellows of an old-fashioned camera,” suggesting that this phenomenon may play an essential role in coronary artery spasm which causes the narrowing of outer diameter. 14) Histological findings in coronary spasm are very similar to those in moyamoya disease. Taken together, we tentatively propose the hypothesis that both luminal stenosis and outer diameter narrowing may simultaneously develop in the carotid forks and initiate moyamoya disease.…”

Multiscale three-dimensional surface reconstruction and surface roughness of porcine left anterior descending coronary arteries

“…Other studies have qualitatively assessed the dehydrated surface of coronary arteries using SEM [35,36], and they have also investigated hydrated samples using scanning force microscopy [35]. Endothelial cells were noted to be aligned longitudinally, as they were within this study, causing ridges along the sample surface [37]. However, none of these studies quantified the surface roughness of arteries, or noted a helical arrangement of ridges.…”

Prediction of Chronic Vessel Enlargement by a Novel Intravascular Ultrasound Finding

“…Recent pathological studies have suggested a possible role of the IEM and media in coronary arterial lesions with spasm or vessel shrinkage. 5, 6 Mortensen et al reported folding of the IEM during coronary spasm. 5 Furthermore, Uchida et al demonstrated both folding of the IEM and thickening of the media during coronary spasm.…”

“…5 Furthermore, Uchida et al demonstrated both folding of the IEM and thickening of the media during coronary spasm. 6 Folding of the IEM may enhance ultrasonic backscatter signal from the luminal border of the media, which is characterized as a low-echoic or sonolucent circular band. Coronary segments distal to the CTO lesion or severe stenosis with delayed distal flow typically show vessel shrinkage because of decreased perfusion pressure and impaired flowmediated vasodilatation.…”